Background: Bronchoalveolar lavage fluid (BALF) lymphocytosis was found in patients with usual interstitial pneumonia (UIP) associated with collagen vascular diseases (CVD) other than diffuse systemic sclerosis (SSc), but it was not found in patients with idiopathic pulmonary fibrosis (IPF), a disease histologically diagnosed as UIP. This difference could be partly due to variations of UIP spectrums between IPF and interstitial pneumonia associated with CVD. Methods: We scored histopathological findings of lung specimens obtained from 31 cases (16 IPF, 9 CVD other than SSc and 6 SSc) using a semiquantitative scoring method. All cases were diagnosed as UIP by surgical lung biopsy. None of the patients were current smokers. Results: Compared with IPF and SSc cases, CVD patients without SSc presented decreased scores of fibrosis (p < 0.01) and alveolar space cellularity (severity, p < 0.05). Lymphocytes were mainly localized in the alveolar walls and the majority of cells in the alveolar spaces were macrophages. On the other hand, other scores such as cellularity and alveolar wall cell infiltrate did not vary among these three groups. Conclusion: Fewer macrophages in the alveolar spaces and a decrease in the degree of fibrosis may contribute to BALF lymphocytosis more in patients with UIP/CVD non-SSc than in patients with IPF/UIP and UIP-SSc.

Background: Chronic smoking influences bronchoalveolar lavage fluid (BALF) cell profiles in healthy subjects, which may alter profiles of inflammatory and regulatory cytokines. Objective: We focused on the evaluation of smoking-related changes in the amounts of cytokines released from BALF macrophages. Methods: We measured the amounts of immunoreactive culture supernatants by using ELISA. Results: The amounts of IL-1 receptor antagonist (IL-1ra) were lower in smokers [n = 10, median 22.1 ng/ml, 25th and 75th percentiles (18.7–39.1)] than in nonsmokers [n = 10, 48.6 (39.2–66.1), p = 0.010]. In smokers, lipopolysaccharide stimulation revealed decreases in the amounts of interleukin-6 (IL-6) [nonsmokers: 2.1 ng/ml (0.68–5.4 vs. smokers: 0.5 (0.03–0.87), p = 0.049] as well as IL-1ra [nonsmokers: 69.2 ng/ml (48.3– 83.8) vs. smokers: 27.3 (17.2–56.7), p = 0.028]. A delay in release from intracellular storage was not the cause of the reduced amounts of IL-1ra. In addition, interleukin-1β (IL-1β) was positively correlated with IL-6 and granulocyte macrophage colony-stimulating factor in nonsmokers, but not in smokers. Furthermore, the decreases in IL-1ra and interleukin-8 were correlated with the increase in the number of BALF macrophages in smokers, but not in nonsmokers. Conclusions: Chronic smoking caused changes in the profiles of cytokines released from BALF macrophages in healthy subjects. Decreases in the amounts of regulatory cytokines, but not prominent changes in the amounts of inflammatory ones, were characteristic.

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A 60-year-old man was treated with rifampicin, isoniazid, ethambutol and pyrazinamide for pulmonary tuberculosis. Acute renal failure developed 1 month after re-administration of rifampicin following 1 month’s interruption of treatment. A renal biopsy showed crescentic lesions characteristic of rapidly progressive glomerulonephritis. This is, to our knowledge, the fourth case of rapidly progressive crescentic glomerulonephritis associated with rifampicin treatment, which responded to methylprednisolone pulse therapy followed by oral steroid therapy.

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